Abstract

Objective: To investigate the role of NF-kB in the mechanism of acute lung injury in rats with acute severe pancreatitis, observed in rats with severe acute pancreatitis with acute lung injury, alveolar macrophage activity, levels of inflammatory cytokines, plasma endotoxin content links and other related indicators of change and Qingyitang different drug treatment, provide new inspiration for the clinical treatment of acute lung injury. Methods: The pancreatic duct retrograde injection of sodium deoxycholate copy of rats with severe acute pancreatitis with acute lung injury model. Qing Yi Tang group therapeutic dose 1ml/100wt, the Sandostatin group therapy dose 20μg/kg dexamethasone group therapeutic dose of 2mg/kg in all treatment groups immediately after modeling time and after modeling 12h again administered. 24h after take specimens for pathological examination and the indicators detected. Meanwhile, by separation and purification of the normal rat lung alveolar macrophages in a concentration of 5 × 10 5 cells seeded in 24-well culture plate. LPS and a variety of drugs, divided into a control group, stimulation group (LPS 10μg/ml), Qingyitang group (LPS Qingyitang). Dexamethasone group (LPS dexamethasone, 100μmol / L), in the role of 3h, 5h, 6h and 24h were used to detect the activity of NF-kB, iNOSmRNA content, TNFα concentration and NO content. Gel electrophoresis mobility shift assay (EMSA) detection alveolar macrophage NF-kB activity and EMSA specificity by reverse transcription - polymerase chain reaction (RT-PCR) detect AM in iNOSmRNA expression, using SDS-poly BALF protein analysis by acrylamide gel electrophoresis. Results: the model of alveolar macrophages excessive activation of NF-kB activity enhancement, iNOSmRNA high expression, TNFα, NO, iNOS was significantly higher than the sham group. Meanwhile, the performance of the model group pathology of lung injury, lung wet / dry ratio, toxins in the blood, blood amylase indicators significantly higher than in the sham group (p <0.01). Qingyitang, dexamethasone, Sandostatin can downregulate the activity of NF-kB to reduce iNOSmRNA expression, to reduce the degree of lung injury, and Kay complex given no obvious role. The Qingyitang group blood endotoxin, TNFα, NO detection indicators decline significantly. The Sandostatin group inhibit blood amylase and alveolar macrophages to secrete inflammatory cytokines strongest. Dexamethasone group to improve lung wet / dry ratio plays a significant role. Vitro normal rat alveolar macrophages after LPS stimulation, the supernatant levels of TNFα, NO, alveolar macrophages of iNOS, content, iNOSmRNA, level, NF-kB activity was significantly higher than that in the control group (P <0.01); Qingyitang group, dexamethasone group was significantly lower than that in the model group (P lt; 0.05). Conclusion: acute severe pancreatitis acute lung injury, stare clothing B activation, then the start of TNF. , INOS, NO Daying expression. Excessive activation of alveolar macrophages, the release of a large number of inflammatory factors lead to high levels of endotoxin in the blood endotoxemia plays a very crucial role in the pathogenesis. The Chinese medicine Qingyitang by down-regulating NF kB activity, reducing the excessive activation of alveolar macrophages to reduce under TN. T the expression of iNOS, NO and inflammatory cytokines, reduce the high levels of endotoxin in the blood and amylase concentration numerous aspects of the regulation of the body play a protective role. Sandostatin, dexamethasone can cut the margin kB activity, impact above certain changes, in order to achieve the protective effect against acute lung injury. Chinese and Western medicines in the different aspects of severe acute pancreatitis acute lung injury, plays a very important role in their own strengths, if Integrative reasonable combination of Chinese and Western medicine, clinical acute pancreatitis will The prevention and treatment of acute lung injury provides a new effective way.